Tanzanian Endemic Optic Neuropathy

Tanzanian Endemic Optic Neuropathy, often shortened to TEON, is a disease that damages the optic nerves in both eyes. The optic nerves are like thick electric cables that carry visual messages from the eyes to the brain. When these nerves do not work well, central vision fades, colors look washed out, and reading becomes hard. In TEON, the problem usually comes on subacutely—not suddenly like an attack, and not over many years, but over weeks to a few months. It affects both eyes, is painless, and mainly involves central vision rather than side (peripheral) vision. Over time, the pale area on the temporal side of the optic disc (the spot where the nerve enters the eye) becomes noticeable, showing loss of fibers that serve the macula (the fine-detail part of vision). TEON has been seen in and around Dar es Salaam on Tanzania’s coast and is considered endemic there, meaning it persists in that population rather than being a one-time outbreak. Studies estimate it affects a small but important percentage of teenagers and young adults, and some patients also have numbness or tingling in the feet and hands (peripheral neuropathy) or reduced hearing. The exact single cause has not been proven; most experts think multiple factors work together in people who are vulnerable. School of MedicinePubMed+1

Tanzanian endemic optic neuropathy (TEON) is a disease that mainly appears in and around Dar es Salaam, Tanzania. It causes gradual, painless, both-eye loss of central vision and poor color vision over weeks to months. Many people also have hearing loss and numbness or burning pain in the feet or hands, which means the problem is not only in the eyes but also in the nerves elsewhere. TEON most often affects teenagers and young adults (about ages 10–39). The disease has been seen in this region since the early 1990s and can affect a noticeable share of young people living there. Scientists have not yet found a single proven cause; instead, TEON seems to happen in people who have nutritional stress and environmental risks. Sadly, once the optic nerve is badly damaged, vision loss can be permanent, so early recognition and supportive care are essential. EyeWikiSchool of Medicine

TEON first drew attention in the late 1980s–1990s in Dar es Salaam and surrounding coastal areas. Over time, it shifted from an epidemic pattern (a surge) to an endemic pattern (a continuing presence). Young people are the most affected group; school surveys and clinic series confirm this age pattern. Population estimates from local research groups and clinic cohorts suggest roughly 0.3% up to about 2.4% of young people may be affected in some communities, which is a substantial health issue for a condition that strikes during school years or early working life. PubMed+1School of Medicine

A simple picture of how the disease behaves in the body

The optic nerve runs on high energy. Cells in the optic nerve rely heavily on mitochondria, the tiny “power plants” in our cells. Anything that upsets mitochondrial function—such as low levels of certain vitamins, oxidative stress, smoke exposure, or genetic vulnerabilities—can push the optic nerve past its safety margin. In TEON, many patients show loss of the papillomacular bundle (the fibers that carry central vision). Modern scans sometimes show microcystic changes in the inner retina, probably a secondary effect of ganglion cell loss. Some patients also have large-fiber and small-fiber peripheral nerve involvement and sensorineural hearing loss, which suggests a broader, energy-related nerve problem in susceptible people. PubMed+1

---

Types

There is no single official international classification. However, for clear communication with patients and for public health planning, doctors often sort TEON into practical types based on the features seen at the eye clinic and in nerve tests. The types below are descriptive and overlapping—a patient can slide from one to another as the disease progresses.

1. Classic optic-nerve–predominant TEON
   This is the common pattern. The patient has a few weeks to months of painless, bilateral central blurring, color vision loss, and reduced contrast sensitivity. Side vision is relatively spared. The optic discs may look slightly hyperemic (flushed) early and later show temporal pallor as fibers die back. PubMed

2. TEON with peripheral neuropathy
   In addition to the eye findings, the patient reports tingling, numbness, burning pain, or reduced vibration sense in the feet and hands. Nerve conduction studies show large-fiber involvement in many such patients, while symptoms can also suggest small-fiber loss. This broader nerve involvement supports the idea of a systemic metabolic/mitochondrial stress. PubMed

3. TEON with sensorineural hearing loss
   Some patients also notice reduced hearing. This hearing loss is usually on the sensorineural side (inner ear/nerve), matching the “energy-hungry nerve” theme seen in the eyes and peripheral nerves. PubMed

4. TEON with microcystic inner-retinal change on OCT
   High-resolution optical coherence tomography (OCT) sometimes shows small cyst-like spaces in the inner nuclear layer, often in an annular pattern on near-infrared en-face views. These changes track with severe thinning of the nerve fiber layer and likely represent secondary changes after ganglion-cell loss. PubMed

5. Severity-graded TEON (by visual acuity)
   Clinicians also talk in terms of mild, moderate, or severe based on best-corrected acuity (for example, can the person still read the 6/9 line, or have they dropped to 6/60?). This helps track progression and plan support even though it does not explain the cause. (General clinical usage; see prevalence/severity context in cohort studies.) PubMed

---

Causes and contributing factors

Important: No single cause explains every case. The best current view is multifactorial risk: nutrition, environment, and individual susceptibility likely combine to injure the optic nerve. Below are 20 factors commonly discussed in the research record. Where evidence is stronger, we say so. Where evidence is uncertain, we explain that too.

1. Low folate (vitamin B9) status — strong case-control evidence
   A Tanzanian case-control study found that higher folate was strongly protective, while low folate increased risk. Folate supports DNA synthesis and mitochondrial one-carbon metabolism; deficiency raises homocysteine, which can injure nerves. PubMed

2. Indoor air pollution from charcoal/firewood smoke — strong association
   Cooking indoors and using charcoal or firewood indoors were each linked with a big increase in risk. Smoke adds oxidative stress and may impair mitochondrial function in susceptible optic nerves. PubMed

3. Low dietary protein intake — protective when higher
   The same study found that higher protein intake reduced risk. Protein supplies essential amino acids for mitochondrial enzymes and antioxidant defenses. PubMed

4. Low sunlight exposure and low vitamin D — plausible, under study
   A registered TEON study highlights low vitamin D and reduced sun exposure as likely contributors, given vitamin D’s role in cell signaling and mitochondrial function, and the potential nitric oxide release from sun-exposed skin that may support cellular energy regulation. isrctn.com

5. General B-vitamin insufficiency (B1, B2, B3, B12) — biologically plausible
   Optic nerve disorders linked to B-vitamin deficits are well described. In TEON, widespread B-vitamin deficiency has been reported in affected areas, though not every study ties a particular vitamin to every patient. These vitamins support mitochondrial energy metabolism. EyeWiki

6. Vitamin B12 deficiency (and raised methylmalonic acid) — mixed evidence
   B12 deficiency can cause a nutritional optic neuropathy. In TEON populations, B12 is part of the work-up, but not all case-control comparisons show a consistent signal. The mechanism (myelin and mitochondrial enzymes) still makes B12 clinically relevant. (General background and TEON protocols.) isrctn.com

7. Thiamine (B1) deficiency — plausible
   Thiamine powers pyruvate dehydrogenase and other enzymes critical for neuronal energy. TEON research explicitly measures thiamine as a candidate factor given the energy needs of optic nerve tissue. isrctn.com

8. Riboflavin (B2) and niacin (B3) shortfalls — plausible
   These vitamins help form FAD and NAD/NADP, core cofactors in electron transport and redox reactions. Deficits can worsen mitochondrial stress in susceptible nerves. (General mechanism; included in broader nutritional frameworks referenced by TEON groups.) isrctn.com

9. Oxidative stress and redox imbalance — active research target
   The TEON protocol measures nitric oxide and thiol-redox biomarkers. A persistent imbalance can harm mitochondria and ganglion cells. isrctn.com

10. Genetic susceptibility (including mitochondrial genes) — likely modifier
    Classic LHON mutations have not explained TEON cases. However, other genetic backgrounds may influence mitochondrial resilience and risk when nutrition or smoke exposure are unfavorable. PubMed

11. Heavy metals (e.g., manganese, cobalt, tin) — possible environmental contributors
    A Tanzanian study of a related multi-sensory neuropathy syndrome in young adults found higher toenail levels of manganese, cobalt, and tin in cases than controls. Toenails reflect prior months of exposure and support considering metals as possible contributors in optic-neuropathy clusters. PMCCDC Stacks

12. Biomass-fuel kitchen exposure in small, poorly ventilated spaces
    This is a more detailed way of stating #2. Fine particles and gases (CO, NOx, aldehydes) in unvented kitchens may chronically injure energy-hungry tissues like the optic nerve. (Risk factor framework from Tanzania study.) PubMed

13. Low antioxidant intake or status
    Diets lacking fruits/vegetables reduce antioxidant vitamins and polyphenols that help buffer oxidative stress. TEON protocols consider the broader diet pattern, not just single vitamins. isrctn.com

14. Rapid urbanization and lifestyle change
    Shifts toward indoor life (less sun), cheaper refined staples, and smoky cooking fuel create a stacked risk profile for susceptible youth. (Context from TEON research summaries.) isrctn.com

15. Poverty and food insecurity
    Lower household resources correlate with TEON in school surveys, likely through diet quality and living conditions (e.g., indoor smoke). PubMed

16. Cassava cyanide exposure — not supported as a main cause in TEON
    Unlike the Cuban epidemic (where cassava-related cyanide was implicated), Tanzanian investigations did not find cyanide poisoning in TEON cases, and common LHON mutations were also absent. This helps narrow the search toward other pathways. PubMed

17. Alcohol and tobacco — general nutritional optic neuropathy risks
    In many settings, heavy alcohol and tobacco use co-occur with poor diet and B-vitamin deficits and can injure the optic nerve. Their exact role in TEON cohorts is less clear but remains biologically plausible and clinically relevant. (Background from broader toxic-nutritional optic neuropathy literature.) MDPI

18. Infections and inflammatory causes — usually not the driver in TEON
    Work-ups assess for infections or demyelination, but TEON patterns and cohorts point away from these as common primary causes, and more toward metabolic/environmental stress in susceptible nerves. (Clinical differentiation discussed in TEON protocols and cohorts.) isrctn.com

19. Micronutrient interactions (e.g., folate-B12-homocysteine triangle)
    When folate or B12 is low, homocysteine rises, harming endothelium and neurons. This shared pathway can amplify other stresses like smoke exposure. (Mechanism consistent with case-control signals for folate.) PubMed

20. Age-specific vulnerability of retinal ganglion cells
    The young adult predominance hints that developing or remodeling neural tissues may be more vulnerable to combined nutritional and environmental stressors, which may explain the age pattern seen in cohorts. (Inference from epidemiology and mitochondrial biology focus.) PubMedisrctn.com

---

Symptoms

1. Blurry central vision in both eyes
   People notice trouble reading, recognizing faces, or seeing small details. Side vision often feels okay at first.

2. Faded or “washed-out” colors
   Colors lose brightness, especially red. This is a hallmark of optic-nerve problems affecting the papillomacular fibers.

3. Painless visual decline
   There is no eye pain. The change creeps in over weeks to a few months, not seconds or years.

4. Worse contrast
   Gray text on a gray background becomes very hard to see; bold, high-contrast text is easier.

5. Central or cecocentral blind spot
   A blank or hazy area sits near the point of fixation. It makes reading across a line of text slow or impossible.

6. Trouble with bright light or dim light tasks
   Going from bright to dim or vice versa can be uncomfortable and slow the eyes down because central vision is weak.

7. No double vision
   The eyes are aligned; the problem is in the signal, not the aim.

8. Normal-looking eyes at first
   Early in the disease, the eyes can look normal to friends and family. Later, the optic disc’s temporal side turns pale.

9. Steady rather than fluctuating vision
   Vision does not swing wildly day to day. It tends to decline and then plateau.

10. Reading fatigue and headaches from eye strain
    Because central vision is weak, reading causes fatigue and sometimes a dull headache from effort.

11. Difficulty distinguishing faces at a distance
    Fine details needed for face recognition live in the macula and are hit early in TEON.

12. Hearing seems “not as sharp” in some people
    A subgroup reports reduced hearing, matching findings of sensorineural hearing loss in clinic cohorts. PubMed

13. Tingling or numbness in feet or hands in some people
    Another subgroup notes peripheral neuropathy symptoms (pins-and-needles, burning, or numbness). PubMed

14. Stable peripheral vision
    Most patients keep side vision, which helps them move around, even while reading remains hard.

15. No redness or discharge
    This is not a surface eye disease. The front of the eye often looks normal.

---

Diagnostic tests

A) Physical exam

1. General nutrition and body assessment
   Doctors check weight, body-mass index, hair and skin quality, mouth (glossitis, stomatitis), and nail lines. This helps spot long-standing nutritional stress that could weaken nerves.

2. Neurologic exam for peripheral neuropathy
   Reflexes, vibration sense, pin-prick, and temperature testing look for nerve fiber loss in the limbs. In TEON cohorts, nearly half can show signs of peripheral neuropathy, supporting a multi-system nerve stress picture. PubMed

3. Simple hearing checks
   A whisper test or tuning fork screening gives a quick sense of sensorineural hearing; formal audiometry often follows if concerns arise. PubMed

4. Gait and balance (Romberg, tandem gait)
   Standing with feet together, eyes closed, or walking heel-to-toe may uncover large-fiber neuropathy that affects balance.

B) Manual eye tests

5. Visual acuity (Snellen or ETDRS)
   Measures the smallest letters you can read with best correction. TEON patients typically show a central acuity drop in both eyes.

6. Color vision (Ishihara or HRR plates)
   TEON causes acquired dyschromatopsia (often red–green first). This is a sensitive sign of optic-nerve dysfunction.

7. Red desaturation (red-cap test)
   A simple cap from dilating drops is shown to each eye. The TEON eye sees the red as less vivid, reflecting papillo-macular bundle injury.

8. Contrast sensitivity (Pelli–Robson chart)
   Patients need stronger contrast to see letters; scores are often reduced in TEON.

9. Confrontation visual fields
   Quick bedside test to detect central or cecocentral scotomas. Full perimetry (automated fields) is usually done later.

10. Pupillary reflex and swinging-flashlight test
    Pupils often look symmetric because both nerves are affected; a relative afferent defect is uncommon unless one eye is much worse.

C) Lab and pathological tests

11. Serum folate and homocysteine
    Low folate and high homocysteine support a one-carbon metabolism deficit that stresses mitochondria; higher folate is protective in Tanzanian data. PubMed

12. Vitamin B12 and methylmalonic acid (MMA)
    Low B12 and high MMA point to a B12-linked neuropathy. Even if not the main driver for every TEON patient, it is important to check and treat if abnormal. (General nutritional optic neuropathy work-up.) MDPI

13. Vitamin D (25-OH vitamin D)
    Low vitamin D fits the low-sunlight hypothesis and is explicitly included in TEON research protocols. isrctn.com

14. Thiamine (B1) level or functional testing
    B1 powers key mitochondrial enzymes. TEON protocols list thiamine among measured micronutrients given its role in energy metabolism. isrctn.com

15. Environmental/toxic screens as indicated
    This can include urinary thiocyanate (to rule cyanide exposure when relevant) and heavy-metal screening (e.g., blood/urine; in research, toenail analysis has linked higher manganese, cobalt, tin to a related Tanzanian neuropathy syndrome). These tests help rule in/out environmental contributors in the local context. PubMedPMC

D) Electrodiagnostic tests

16. Visually Evoked Potentials (VEP)
    Pattern-reversal VEP checks the signal speed and strength from eye to brain. In TEON, VEPs often show optic-nerve pathway dysfunction consistent with the clinical picture. PubMed

17. Pattern Electroretinogram (PERG) or full-field ERG
    These assess retinal ganglion cell function (PERG) and global retinal activity (ERG). TEON series have shown optic-nerve–dominant dysfunction, though limited primary retinal involvement can appear in some cases. PubMed

18. Nerve conduction studies (± Brainstem Auditory Evoked Responses)
    Peripheral nerve conduction testing documents large-fiber neuropathy in a notable fraction of patients. BAER/ABR can support sensorineural hearing involvement. PubMed

E) Imaging tests

19. Optical Coherence Tomography (OCT) with near-infrared en-face views
    OCT measures the thickness of the retinal nerve fiber layer (RNFL) and ganglion cell complex. In TEON, there is often severe, symmetric thinning of fibers serving the macula (papillomacular bundle). Some patients show microcystic inner-retinal changes that align with areas of severe nerve fiber loss. Near-infrared en-face imaging can highlight an annular pattern not obvious on color photos. PubMed

20. MRI of brain and orbits (with contrast when needed)
    MRI helps exclude other causes of optic neuropathy (compressive lesions, demyelination). In TEON, MRI is typically unremarkable for structural lesions but remains important to make sure nothing else is missed. (General neuro-ophthalmic practice; TEON cohorts rely on clinical and electrophysiologic patterns rather than MRI findings.) PubMed

Non-pharmacological treatments

1. Nutrition counseling & meal planning — personalize affordable, locally available foods to correct folate/B-vitamin/protein gaps; purpose: halt ongoing deficiency; mechanism: restores cofactors for myelin and mitochondrial energy. PMC

2. Dietary diversity program — add legumes, dark leafy greens, citrus, fortified grains, eggs, fish, dairy or other culturally acceptable B12 sources; purpose: broaden micronutrient intake; mechanism: supports nerve metabolism. PMC

3. Cooking-smoke reduction — cook outdoors or improve ventilation/chimneys; purpose: reduce indoor pollution; mechanism: lowers oxidative/toxic stress. PubMed

4. Tobacco cessation — counseling plus support; purpose: remove a key toxin; mechanism: reduces oxidative stress and nutrient depletion. PMC

5. Alcohol-use counseling — brief interventions; purpose: cut a major driver of malnutrition; mechanism: improves nutrient absorption and mitochondria function. PMC

6. Low-vision rehabilitation — referral early; purpose: maximize remaining vision; mechanism: training + devices offset central scotomas.

7. High-contrast/lighting optimization at home/school — brighter task lights, glare control; purpose: improve readability; mechanism: boosts signal for damaged pathways.

8. Optical aids — strong reading glasses, handheld stand magnifiers, electronic magnifiers; purpose: enlarge print; mechanism: shift reading toward healthier retinal areas.

9. Eccentric viewing training — learn to look slightly off-center; purpose: bypass the central scotoma; mechanism: uses intact parafoveal retina.

10. Assistive technology — screen readers, text-to-speech, large-print settings; purpose: maintain education/employment.

11. Orientation & mobility coaching — safe navigation skills; purpose: independence and fall prevention.

12. Hearing assessment & rehabilitation — audiology referral; purpose: improve communication when hearing loss co-exists. EyeWiki

13. Foot care & neuropathy self-care — footwear, daily checks; purpose: protect numb feet from injury.

14. Micronutrient-rich school meals — in communities with TEON; purpose/mechanism: add B-vitamins and protein for at-risk ages.

15. Community health education — simple messages on diet diversity, smoke exposure, and early eye checks.

16. Mental-health support — address depression/anxiety after vision loss; purpose: improve quality of life and adherence.

17. Sleep hygiene & stress control — supports neuro-recovery; mechanism: reduces systemic oxidative stress.

18. Safe food-processing practices — although cyanide not proven in TEON, good processing of cassava and adequate protein intake are smart for general neuro-nutrition. EyeWiki

19. Sun/UV comfort strategies — hats, shaded work areas; purpose: reduce light discomfort.

20. Regular follow-up schedule — early weeks: frequent checks; later: every few months; purpose: track vision, reinforce nutrition, adjust aids. PMC

---

Drug treatments

Important: Doses below reflect common clinical references for deficiency states in adults, not a one-size-fits-all TEON prescription. Your clinician will tailor them to labs, age, pregnancy, comorbidities, and local protocols.

1. Vitamin B12 (cobalamin) — class: water-soluble vitamin
   Dose/time (examples): IM cyanocobalamin 1000 µg weekly ×4, then monthly; or oral 1–2 mg daily when absorption is intact.
   Purpose: correct/prevent B12-related optic neuropathy.
   Mechanism: restores myelin and mitochondrial reactions (methylmalonyl-CoA → succinyl-CoA; homocysteine → methionine).
   Side effects: very rare (injection-site pain). Monitor B12/MMA. AAFP

2. Folic acid (vitamin B9)
   Dose/time (examples): 1–5 mg orally daily for months until recovery and cause corrected.
   Purpose: treat folate-deficiency optic neuropathy and anemia.
   Mechanism: restores one-carbon metabolism for DNA/myelin; lowers homocysteine.
   Side effects/caution: do not give high-dose folate alone if B12 deficiency is possible—can mask anemia while neurologic damage continues. PubMedEyeWiki

3. Thiamine (vitamin B1)
   Dose/time (examples): ranges from 100–200 mg IV daily for 3 days then 100 mg orally daily in deficiency states; higher IV doses used when Wernicke encephalopathy suspected.
   Purpose: support mitochondrial energy (especially in malnutrition/alcohol use).
   Mechanism: cofactor for pyruvate dehydrogenase; boosts ATP for retinal ganglion cells.
   Side effects: rare; give magnesium if low. Life in the Fast Lane • LITFL

4. Copper supplementation
   Dose/time (example per review): IV copper sulfate ~2.4 mg in 100 mL NS daily for 5 days, then oral copper gluconate 2 mg q6h; tailor to labs.
   Purpose: treat copper-deficiency myeloneuropathy/optic neuropathy.
   Mechanism: restores cupro-enzymes for myelin and mitochondrial function.
   Side effects: GI upset, risk of overload—monitor levels. PMC

5. Riboflavin (B2) (adjunct when diet is poor)
   Dose/time: often 5–10 mg/day in multivitamin regimens.
   Purpose: supports redox enzymes in mitochondria.
   Mechanism: precursor for FAD/FMN, aiding electron transport.
   Side effects: bright-yellow urine (benign). PMC

6. Niacin (B3) (adjunct; avoid flush-prone high doses without supervision)
   Dose/time: nutritional doses per multivitamin; high-dose niacin for lipids is not a TEON treatment.
   Purpose/mechanism: NAD/NADP coenzymes support energy reactions.
   Side effects: flushing, liver enzymes at high doses. PMC

7. Pyridoxine (B6) (adjunct)
   Dose/time: nutritional doses; avoid chronic megadoses (>100 mg/day) that can cause neuropathy.
   Purpose/mechanism: cofactor for neurotransmitter and myelin metabolism.
   Side effects: sensory neuropathy at high doses. PMC

8. Multivitamin/mineral (with B-complex + trace minerals)
   Dose/time: as labeled daily.
   Purpose: broad safety net when diet is unreliable.
   Mechanism: reduces multi-micronutrient gaps contributing to neuropathy. PMC

9. Smoking-cessation pharmacotherapy — nicotine replacement, bupropion, or varenicline (fit to patient)
   Purpose: remove a toxin and improve nutrition recovery.
   Mechanism: supports abstinence; reduces oxidative stress input to the optic nerve.
   Side effects: depend on agent; review contraindications.

10. Alcohol-use disorder medications — naltrexone, acamprosate (when indicated)
    Purpose: reduce relapse and improve nutrition/absorption.
    Mechanism: neurochemical support for abstinence.
    Side effects: liver/kidney considerations; clinician-guided.

Note: Some mitochondrial optic neuropathies (like LHON) use idebenone (a CoQ10 analog) off-label. It has supportive evidence in LHON, but TEON is different, and idebenone is not an established TEON therapy. Consider clinical trials only if available. PMCNHS England

---

Dietary molecular supplements

These do not replace vitamin treatment for true deficiencies. They are optional supports discussed with your clinician.

1. Coenzyme Q10 (ubiquinone) — 100–200 mg/day; function: mitochondrial electron shuttle; mechanism: supports ATP and reduces oxidative stress.

2. Alpha-lipoic acid — 300–600 mg/day; function: antioxidant used in neuropathy care; mechanism: scavenges free radicals, may improve nerve conduction.

3. Omega-3 fatty acids (EPA/DHA) — 1–2 g/day; function: anti-inflammatory; mechanism: membrane stabilization for neurons.

4. N-acetylcysteine (NAC) — 600–1200 mg/day; function: glutathione precursor; mechanism: boosts intracellular antioxidants.

5. Vitamin C — 250–500 mg/day; function: antioxidant; mechanism: reduces oxidative stress.

6. Vitamin E — 100–200 IU/day; function: lipid antioxidant; mechanism: protects membranes.

7. Lutein/zeaxanthin — label doses; function: macular pigment support; mechanism: filters blue light/antioxidant at retina.

8. Taurine — 500–1000 mg/day; function: retinal/neuronal osmoprotection; mechanism: modulates calcium and oxidative stress.

9. Magnesium — 200–400 mg/day (if low); function: cofactor in energy enzymes; mechanism: supports thiamine-dependent reactions.

10. Zinc/copper balanced — only if low; function: enzyme cofactors; mechanism: supports antioxidant enzymes; warning: excess zinc can cause copper deficiency—avoid unsupervised megadoses.

---

Regenerative, or stem-cell drugs

There are no approved immune-booster drugs, stem-cell drugs, or regenerative medicines proven to restore vision in TEON. The best-supported approach is early identification, correction of nutritional deficiencies (B12, folate, thiamine, copper), and risk-factor reduction. Experimental neuroprotectives like idebenone apply to LHON and do not have established benefit in TEON; they should not be used outside clinical trials. EyeWikiPMC+1

---

Surgery:

• Bottom line: There is no surgery that repairs the optic nerve damage in TEON. Operations like cataract surgery, optic-nerve sheath fenestration, or retinal surgeries target other diseases and do not reverse the central vision loss pattern of TEON. The effective “rehabilitation pathway” is non-surgical (low-vision aids, training, environmental changes) while clinicians treat deficiencies and risks. EyeWiki

---

Prevention

1. Eat a diverse diet that includes folate-rich greens/legumes and reliable B12 sources (eggs, dairy, fish, meat or fortified foods). PMC

2. Improve kitchen ventilation; avoid heavy indoor smoke. Cook outside when possible. PubMed

3. Don’t smoke; seek help to quit. PMC

4. Limit alcohol; get support for dependence. PMC

5. Use fortified staples when available; take supervised vitamins during high-risk periods (pregnancy, illness, restricted diets). PMC

6. Routine vision screening in schools/young adults in affected areas.

7. Early clinic visits for any new central blur or color-vision change.

8. Occupational/environmental safety to reduce heavy-metal exposure. EyeWiki

9. Community nutrition programs (school meals, local legumes, small-animal protein, fish).

10. General safe food processing; although cyanide wasn’t implicated in TEON, good cassava processing and adequate protein are wise for nerve health. EyeWiki

---

When to see a doctor (immediately)

• You notice new blur in the center of vision in either/both eyes.

• Colors look wrong/faded, or reading becomes suddenly difficult.

• You develop tingling/burning in feet or hands, or hearing worsens.

• You follow a diet low in B-vitamins or protein, or have GI disease/surgery that limits absorption.

• You smoke or drink heavily and have any of the symptoms above.

• Any child/teen in an affected area develops central vision problems.

Early care matters because vitamin supplementation helps most when started early. EyeWiki

---

Foods to prioritize

Eat more of (as available and culturally acceptable):

1. Dark leafy greens (amaranth leaves, spinach) — folate.

2. Beans/peas/lentils/groundnuts — folate, protein.

3. Eggs — B12, protein.

4. Milk/yoghurt/cheese — B12, protein.

5. Fish (freshwater/marine) — B12, protein, omega-3s.

6. Organ meats (where acceptable) — rich B12.

7. Fortified flours/cereals — added B-vitamins.

8. Citrus/guava/mango — vitamin C aids absorption.

9. Seeds/nuts — minerals, healthy fats.

10. Varied vegetables — broad micronutrient coverage.

Limit/avoid:

1. Tobacco in any form.

2. Heavy alcohol.

3. Unventilated indoor cooking (move stoves, open windows, add chimneys).

4. Ultra-refined staples with little micronutrient content (unless fortified).

5. Megadose zinc without copper monitoring.

6. Self-prescribed megadose B6 (>100 mg/day) long-term.

7. Crash diets that cut out key food groups.

8. Unproven “vision cures” sold online.

9. Lead-glazed/unsafe cookware (heavy-metal risk).

10. Reliance on a single staple without diversity (even though cassava cyanide wasn’t implicated in TEON, a monotonous diet raises deficiency risk). EyeWikiPMC

---

Frequently Asked Questions

1. Is TEON contagious?
   No. It is not an infection that spreads between people.

2. Can TEON be cured with a pill?
   There is no single curative pill. Early vitamin therapy and risk-reduction can help, especially if started before severe nerve damage. EyeWiki

3. Will glasses fix it?
   Glasses correct refractive error, not optic-nerve damage. Low-vision aids can still help you function better.

4. Why are colors affected so much?
   The disease targets the papillomacular bundle, which carries central and color information. PubMed

5. Why both eyes together?
   Nutrition/toxin stresses and mitochondrial issues usually affect both eyes symmetrically. PMC

6. Is it the same as LHON (Leber’s)?
   No. TEON does not show common LHON mutations, and its risk factors are different. EyeWiki

7. Is cassava the cause?
   In TEON studies, cyanide poisoning was not found. Still, balanced diets and safe food processing are smart. EyeWiki

8. Does indoor smoke really matter?
   Yes—studies in Dar es Salaam linked indoor smoke and low folate to higher TEON risk. PubMed

9. Can vitamins reverse the vision loss?
   They can help early. Advanced damage may be permanent; that’s why early care is crucial. EyeWiki

10. Which vitamin is the most important?
    It depends on your lab results. Often folate, B12, thiamine, copper are checked and corrected together. PMC

11. Is idebenone useful?
    It’s used for LHON, not proven for TEON. Consider only in clinical trials. PMC

12. Do I need scans?
    Most people get OCT; some need MRI to rule out other causes if something looks unusual. PubMedEyeWiki

13. Are children affected?
    Yes—school-age children have been reported in Dar es Salaam, so screening matters. EyeWiki

14. What if labs are normal?
    Doctors still consider diet, smoke exposure, and other toxins, and they may repeat tests or broaden the work-up.

15. What is the long-term outlook?
    If caught early and nutrition/risks are fixed, some stabilize or improve. If late, damage can be irreversible—hence early care and rehab. EyeWiki

Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical  history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.

The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members

Last Updated: August 27, 2025.